Year in Review | Published:


Fuelling cancer cells

Nature Reviews Endocrinologyvolume 15pages7172 (2019) | Download Citation

Cancer cells consume and utilize glucose at a higher rate than normal cells. However, some microenvironments limit the availability of nutrients and glucose. In 2018, researchers found that tumours depend on a variety of different nutrient sources, both locally and systemically, to overcome metabolic limitations and promote tumour progression and metastasis.

Key advances

  • Lactate, not glucose, is a main carbon source for tricarboxylic acid (TCA) cycle oxidation in tumour cells1,2.

  • Leukaemic cells induce whole-body insulin resistance to increase glucose availability for their growth5.

  • Prostate cancer cells consume necrotic cell debris under both nutrient-replete and nutrient-depleted conditions6.

  • Many tumours become dependent on aspartate for continued growth in hypoxic environments7,8.

  • Asparagine is required for protein synthesis in glutamine-deprived conditions9 and promotes metastasis via epithelial–mesenchymal transition protein synthesis10.

Access optionsAccess options

Rent or Buy article

Get time limited or full article access on ReadCube.


All prices are NET prices.


  1. 1.

    Hui, S. et al. Glucose feeds the TCA cycle via circulating lactate. Nature 551, 115–118 (2017).

  2. 2.

    Faubert, B. et al. Lactate metabolism in human lung tumors. Cell 171, 358–371 (2017).

  3. 3.

    Corbet, C. et al. Interruption of lactate uptake by inhibiting mitochondrial pyruvate transport unravels direct antitumor and radiosensitizing effects. Nat. Commun. 9, 1208 (2018).

  4. 4.

    Chen, Y.-J. et al. Lactate metabolism is associated with mammalian mitochondria. Nat. Chem. Biol. 12, 937–943 (2016).

  5. 5.

    Ye, H. et al. Subversion of systemic glucose metabolism as a mechanism to support the growth of leukemia cells. Cancer Cell 34, 659–673 (2018).

  6. 6.

    Kim, S. M. et al. PTEN deficiency and AMPK activation promote nutrient scavenging and anabolism in prostate cancer cells. Cancer Discov. 8, 866–883 (2018).

  7. 7.

    Garcia-Bermudez, J. et al. Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. Nat. Cell Biol. 20, 775–781 (2018).

  8. 8.

    Sullivan, L. B. et al. Aspartate is an endogenous metabolic limitation for tumour growth. Nat. Cell Biol. 20, 782–788 (2018).

  9. 9.

    Pavlova, N. N. et al. As extracellular glutamine levels decline, asparagine becomes an essential amino acid. Cell Metab. 27, 428–438 (2018).

  10. 10.

    Knott, S. R. V. et al. Asparagine bioavailability governs metastasis in a model of breast cancer. Nature 554, 378–381 (2018).

Download references


The authors’ research is supported by NIH grants R01AG016927, R01CA090764 and R01CA206167 (N.H.), by VA grant BX000733 (N.H.) and by F30CA225058 NIH award (A.R.T.).

Author information


  1. Department of Biochemistry and Molecular Genetics, College of Medicine, University of Illinois at Chicago, Chicago, IL, USA

    • Alexander R. Terry
    •  & Nissim Hay
  2. Research & Development Section, Jesse Brown VA Medical Center, Chicago, IL, USA

    • Nissim Hay


  1. Search for Alexander R. Terry in:

  2. Search for Nissim Hay in:

Competing interests

The authors declare no competing interests.

Corresponding author

Correspondence to Nissim Hay.

About this article

Publication history



Newsletter Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing